Pulmonary toxicity assessment of polypropylene, polystyrene, and polyethylene microplastic fragments in mice

Isaac Kwabena Danso; Jong-Hwan Woo; Seung Hoon Baek; Kilsoo Kim; Kyuhong Lee

doi:10.1007/s43188-023-00224-x

Pulmonary toxicity assessment of polypropylene, polystyrene, and polyethylene microplastic fragments in mice

Toxicol Res. 2024 Mar 8;40(2):313-323. doi: 10.1007/s43188-023-00224-x. eCollection 2024 Apr.

Authors

Isaac Kwabena Danso^{1

2}, Jong-Hwan Woo^{1

3}, Seung Hoon Baek^{1

2}, Kilsoo Kim^{4

5}, Kyuhong Lee^{1

2}

Affiliations

¹ Inhalation Toxicology Center for Airborne Risk Factor, Korea Institute of Toxicology, 30 Baehak1-Gil, Jeongeup, Jeollabuk-do 56212 Republic of Korea.
² Department of Human and Environmental Toxicology, Korea National University of Science & Technology, Daejeon, 34113 Republic of Korea.
³ Biosafety Research Institute and Laboratory of Pathology, College of Veterinary Medicine, Jeonbuk National University, Jeollabuk do, Iksan-si, Republic of Korea.
⁴ Preclinical Research Center, Daegu-Gyeongbuk Medical Innovation Foundation, Daegu, 41061 Republic of Korea.
⁵ College of Veterinary Medicine, Kyungpook National University, 80 Daehakro, Buk-Gu, Daegu, 41566 Republic of Korea.

Abstract

Polypropylene (PP), polystyrene (PS), and polyethylene (PE) plastics are commonly used in household items such as electronic housings, food packaging, bottles, bags, toys, and roofing membranes. The presence of inhalable microplastics in indoor air has become a topic of concern as many people spent extended periods of time indoors during the COVID-19 pandemic lockdown restrictions, however, the toxic effects on the respiratory system are not properly understood. We examined the toxicity of PP, PS, and PE microplastic fragments in the pulmonary system of C57BL/6 mice. For 14 days, mice were intratracheally instilled 5 mg/kg PP, PS, and PE daily. The number of inflammatory cells such as macrophages, neutrophils, and eosinophils in the bronchoalveolar lavage fluid (BALF) of PS-instilled mice was significantly higher than that in the vehicle control (VC). The levels of inflammatory cytokines and chemokines in BALF of PS-instilled mice increased compared to the VC. However, the inflammatory responses in PP- and PE-stimulated mice were not significantly different from those in the VC group. We observed elevated protein levels of toll-like receptor (TLR) 2 in the lung tissue of PP-instilled mice and TLR4 in the lung tissue of PS-instilled mice compared with those to the VC, while TLR1, TLR5, and TLR6 protein levels remained unchanged. Phosphorylation of nuclear factor kappa B (NF-κB) and IĸB-α increased significantly in PS-instilled mice compared with that in VC. Furthermore, Nucleotide‑binding oligomerization domain‑like receptor family pyrin domain‑containing 3 (NLRP3) inflammasome components including NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and Caspase-1 in the lung tissue of PS-instilled mice increased compared with that in the VC, but not in PP- and PE-instilled mice. These results suggest that PS microplastic fragment stimulation induces pulmonary inflammation due to NF-ĸB and NLRP3 inflammasome activation by the TLR4 pathway.

Supplementary information: The online version contains supplementary material available at 10.1007/s43188-023-00224-x.

Keywords: Fragment; Microplastic; NF-ĸB; NLRP3 inflammasome; TLR4.